Predictors of sustained ventricular tachycardia inducibility in patients with nonsustained ventricular tachycardia and chronic coronary artery disease

To assess the likelihood of inducing sustained ventricular tachycardia, we analyzed a cohort of 58 retrospective and 18 prospective patients with chronic coronary artery disease who underwent electrophysiologic study because of spontaneous nonsustained ventricular tachycardia (three or more beats, lasting less than 30 seconds, at a rate greater than 100/min). In 24 of the 58 retrospective patients (41%) sustained ventricular tachycardia was inducible. Stepwise logistic regression identified two "major" variables--left ventricular aneurysm/dyskinesis/akinesis (p = 0.0001; relative risk = 11.88) and ejection fraction less than 40% (p = 0.0002; relative risk = 9.69)--and one "minor" variable--nonsustained ventricular tachycardia longer than 10 beats (p = 0.0151; relative risk = 4.21)--as significant predictors of inducibility. Nineteen patients with both major variables had a high probability of inducibility (greater than 90%). Nineteen patients with neither major variable had a low probability of inducibility (less than 5%). The remaining 20 patients with only one of the major variables had an intermediate probability of inducibility (14% to 75%). The significance of the third minor factor, nonsustained ventricular tachycardia longer than 10 beats, was confined to this intermediate group, in which it could be used to segregate relatively high (65% to 75%) and relatively low (14% to 20%) probability of inducibility. Prospective application of the predictor function stratified 18 additional patients into three groups with high (six patients), intermediate (seven patients), and low (five patients) probability of inducibility. The observed rate of inducibility in each group was 5 of 6 (83%), 2 of 7 (29%), and 0 of 5 (0%), respectively. These data suggest that patients with nonsustained ventricular tachycardia and chronic coronary artery disease can be stratified into subgroups with high, intermediate, and low probability of inducibility of sustained ventricular tachycardia on the basis of ejection fraction and regional ventricular wall motion defects alone.     

冠心病持续性室性心动过速患者的Q—T离散度

为评价Q-T_d对冠心病患者发生室性心动过速的预测价值,观察18例冠心病持续性室性心动过速患者和20例对照组的Q-T_d。结果显示持续型室性心动过速组Q_(Td)(104±28ms)明显大于对照组(61±19ms,P<0.01)。表明Q-T_d的增加可作为预测室性心动过速发生的重要指标。     

Cryoablation of refractory sustained ventricular tachycardia due to coronary artery disease

Thirty-nine patients with medically refractory sustained monomorphic ventricular tachycardia (VT) due to coronary artery disease underwent map-guided cryosurgery. Locations of prior myocardial infarctions had been inferior in 22, anterior in 16 and combined in 1. Mean age was 61 +/- 9 years and the mean number of drug trials per patient before surgery was 3.8 +/- 1.4. Intraoperative endocardial mapping induced 67 tachycardias in 35 patients. Each patient received 6 to 18 (11 +/- 3) endocardial cryothermic applications (15 mm, -60 degrees C, 2 minutes) at areas of earliest activation during VT. Encircling endocardial cryoablation was performed in 4 patients who had unsuccessful mapping. In addition, 11 patients had subendocardial resection of their well-demarcated septal scars as well as cryosurgery. There were 2 in-hospital deaths. At postoperative programmed ventricular stimulation, 28 of the 37 patients (76%) had no inducible or spontaneous VT before hospital discharge. Six patients (16%) with spontaneous or inducible VT had a single morphology and were controlled with antiarrhythmic drugs that had previously failed. Therefore, surgery alone or in combination with drugs was efficacious in 92% of the population surviving surgery. The remaining 3 patients (8%) received automatic implantable cardioverter defibrillators. No significant difference in surgical outcome was seen between patients who had cryosurgery alone and those who had subendocardial resection together with cryoablation. Mean left ventricular ejection fractions before and after surgery were 33 and 39%, respectively (p less than 0.01). Clinical follow-up ranged from 2 to 36 months (18 +/- 12). One patient died of heart failure and another underwent heart transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modification of ventricular tachycardia by procainamide in patients with coronary artery disease

Fifteen consecutive patients with coronary artery disease had rapid (158 to 272 beats/min) and sustained ventricular tachycardia induced by the extrastimulus technique, and received procainamide infusion. Before the study, all but one patient had severe symptoms with tachycardia, and six had survived apparent sudden death. Procainamide consistently slowed ventricular tachycardia. However, in traditional doses (1 g infusion, plasma concentration greater than 4 μg/ml), it prevented induction of ventricular tachycardia in only 2 of the 15 patients. Induction of ventricular tachycardia was facilitated by procainamide in 10 patients. Larger doses of procainamide (plasma concentration 20.2 μg/ml ± 9.7 [mean ± standard deviation]) prevented induction of ventricular tachycardia in one of eight patients. Rapid ventricular rates (more than 210 beats/min) that were not slowed (by 50 percent or more) after a 1 g infusion of the drug predicted failure of procainamide to prevent ventricular tachycardia. Therefore, procainamide slowed but did not prevent induced ventricular tachycardia in most of these patients with coronary artery disease at risk of sudden death.     

Ablation of ventricular tachycardia

Ablation is an important management tool for the treatment of ventricular arrhythmias. Even at experienced centers ventricular tachycardia ablation carries a minor but significant risk for potential complications, including vascular and thromboembolic complications, air embolism, volume overload and the precipitation of congestive heart failure, cardiac tamponade from catheter perforation or from steam pop with RF energy delivery, valve or subvalvular support structure disruption, conduction system disruption with development of heart block, coronary artery injury when ablating in the coronary cusps region or trying to gain access to the LV chamber, precipitation of cardiogenic shock from ablation of viable myocardium in patients with marginal reserve and failure to resuscitate or precipitation of cardiogenic shock from repeated VT induction, and with epicardial ablation the potential complications of epicardial access, coronary arteries and phrenic nerve damage. Recognition of these risks is paramount for their avoidance with careful pre-procedure planning and intraprocedural technique being essential to minimize the potential for complications.     

Argon laser ablation of malignant ventricular tachycardia associated with coronary artery disease

The long-term clinical efficacy and safety of intraoperative mapping-guided argon laser ablation alone or in conjunction with standard surgical methods were assessed in 20 consecutive patients with refractory sustained ventricular tachycardia (VT) or ventricular fibrillation. A 15-W argon ion gas laser was used and pulsed laser energy was delivered through a fiberoptic catheter delivery system. Pre- and intraoperative mapping was used to localize the arrhythmogenic tissue. Postoperative clinical, ambulatory electrocardiographic and electrophysiologic evaluations were performed before discharge and at 1 year of follow-up. Thirty-eight VT morphologies were mapped and ablated with laser energy alone (82%), combined laser ablation and mechanical resection (13%) or mechanical resection alone (5%). Concomitant coronary artery bypass surgery was performed in 15 patients and in 1 patient it was performed with mitral value replacement. Postoperative 30-day mortality was 5%. One patient (5%) required postoperative antiarrhythmic drug therapy, and all survivors had suppression of inducible sustained VT at discharge. Mean left ventricular ejection fraction increased from 34 +/- 12% preoperatively to 41 +/- 13% postoperatively (p = 0.001). Efficacy rates for ablation of VT sites associated with anterior myocardial infarction and inferior or posterior myocardial infarction were comparable (100 vs 96%, respectively, p greater than 0.2). At 1-year follow-up no sudden deaths had occurred and total survival rate was 90%. Intraoperative pulsed argon laser ablation alone or in conjunction with standard surgical techniques improves the efficacy of surgical ablation procedures for VT or ventricular fibrillation and reduces the need for additional postoperative antiarrhythmic drug or device therapy.     

Transmural ventricular activation during consecutive cycles of sustained ventricular tachycardia associated with coronary artery disease

Although computerized mapping has enabled the intraoperative delineation of global ventricular activation from a single complex of ventricular tachycardia (VT), beat-to-beat reproducibility of isochronic maps has not been defined. To determine the reliability of single-beat analysis, epicardial and transmural ventricular electrograms during 6 consecutive VT cycles were analyzed in 10 patients during intraoperative mapping of sustained monomorphic VT. Bipolar electrograms were recorded simultaneously using sock and needle electrodes from up to 96 epicardial and 156 transmural sites. In each patient, at each electrode site, local activation time, electrogram duration and morphology were compared over 6 consecutive beats. A total of 9,816 electrograms were analyzed. For each patient, the isochronic activation map during VT was reproducible. Mean beat-to-beat variations in local epicardial and transmural activation times were only 1.7 +/- 1.7 and 2.04 +/- 1.9 ms, respectively (difference not significant). Moreover, electrogram duration did not vary significantly. Mean variations in epicardial and transmural electrogram durations were 2.1 +/- 1.8 and 1.4 +/- 1.9 ms, respectively (difference not significant). There were only 2 instances of 2:1 conduction failure; both occurred intramurally and adjacent to a site of VT origin. Thus, transmural ventricular activation during sustained monomorphic VT is reproducible regardless of electrode site or electrogram duration. These results demonstrate that analysis of a single beat of VT is a reliable and expedient method to delineate ventricular activation during intraoperative computerized mapping for the purpose of clinical decision-making in patients with sustained monomorphic VT.     

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use-dependent electrophysiologic effects of amiodarone in coronary artery disease and inducible ventricular tachycardia.

Amiodarone produces use-dependent block of cardiac sodium channels in vitro. This study assessed whether similar use-dependent block occurred in 19 patients with coronary artery disease and inducible, sustained, monomorphic ventricular tachycardia treated with amiodarone. Beat-to-beat measurements of ventricular paced QRS durations during 12-beat trains at cycle lengths of 700, 600, 400 and 300 ms were analyzed at a baseline antiarrhythmic drug-free study and after 2 and 10 weeks of amiodarone therapy. At the drug-free study, there were no significant changes in paced QRS durations within the 12-beat trains at any pacing cycle lengths. After 2 and 10 weeks of amiodarone therapy, progressive prolongation of paced QRS durations occurred over the 12-beat trains at pacing cycle lengths of 600, 400 and 300 ms (p less than 0.05). Significant changes in QRS duration were not observed at a pacing cycle length of 700 ms. This progressive prolongation in QRS duration can be fitted as a function of beat number to a monoexponential equation and occurred with an onset time constant of 1.02 +/- 0.41 beats (306 +/- 122 ms) at a pacing cycle length of 300 ms. The magnitude of QRS prolongation increased as the pacing cycle length was shortened. The magnitudes of QRS prolongation were similar after 2 and 10 weeks of amiodarone therapy. In conclusion, use-dependent prolongation in QRS duration occurs at rapid pacing cycle lengths in humans receiving amiodarone.     

Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.     

Serial chest thumps for the treatment of ventricular tachycardia in patients with coronary artery disease.

Based on excellent results of successive single chest thumping (CT) and serial chest thumping (SCT) for the interruption of ventricular tachycardia (VT) in experimental animals with subacute myocardial infarction, the SCT method was applied for the treatment of VT in patients with coronary artery disease (CAD). SCT was successful in terminating 13 of 19 episodes of VT (68%) in 8 of 14 patients (57%). Conversion of VT was immediate in 9 episodes in 6 patients and latent in 4 episodes in 2 patients. Complications were rare but significant. In one case, SCT resulted in a ventricular asystole and in another case SCT accelerated the rate of VT from 167/min to 242/min, requiring electroconversion. Neither a short duration of VT nor a preserved left ventricular function seemed to enhance conversion by SCT. For interruption of VT in patients with CAD, SCT is not as successful as in the experimental animal model and, therefore, should not be used as a routine method. It may be applied in selected patients under hospital conditions with a standby defibrillator.     

Ablation of ventricular fibrillation and tachycardia

Catheter ablation therapy for ventricular tachycardia has evolved over the past 20 years to become the first-line therapy. This development has been facilitated by technology that has allowed better anatomic and electrophysiologic correlations. A better understanding of radiofrequency (RF) ablation has led to safer and more effective treatments, allowing it to become a potent diagnostic and therapeutic tool in clinical cardiac electrophysiology. As more knowledge is gained about the mechanisms of arrhythmias through RF ablations, and better mapping technology and more effective methods for energy delivery become available, catheter ablation will become relevant for an increasing number of arrhythmias. This article addresses advances and applications of RF ablation to the treatment of ventricular arrhythmias in a variety of heart diseases.